ArticleFrontiers in cardiovascular medicine2024
CD36 restricts lipid-associated macrophages accumulation in white adipose tissues during atherogenesis.
Article in Frontiers in cardiovascular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Trial
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Lipid-Associated Macrophages in Obesity: Immunometabolic Programs and Emerging Therapeutic Implications-A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.bioRxiv : the preprint server for biology · 2025Article
- Article
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Authors and funding
19 authors.
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Abstract
Visceral white adipose tissues (WAT) regulate systemic lipid metabolism and inflammation. Dysfunctional WAT drive chronic inflammation and facilitate atherosclerosis. Adipose tissue-associated macrophages (ATM) are the predominant immune cells in WAT, but their heterogeneity and phenotypes are poorly defined during atherogenesis. The scavenger receptor CD36 mediates ATM crosstalk with other adipose tissue cells, driving chronic inflammation. Here, we combined the single-cell RNA sequencing technique with cell metabolic and functional assays on major WAT ATM subpopulations using a diet-induced atherosclerosis mouse model (
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